Human Toxic Chemical Exposure - Perchloroethylene

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Reference Summary

Perchloroethylene, also known as tetrachloroethylene, "perc" or PCE, is a chlorinated hydrocarbon solvent. The major uses of PCE are in textile and dry cleaning industries (69%) and metal degreasing (l6%). It is also used in the treatment of intestinal worms. PCE has the following structure:



Acute exposure to PCE may cause central nervous system depression and hepatic injury. Also, chronic low level exposure is known to cause impairment of brain function and decreased memory(l).

PCE has been shown to cause cancer in laboratory animals at exposure levels close to the level now legally allowed in the workplace (2). The animals developed cancer after they were exposed to 100 ppm of PCE for 6 hours per day, 5 days a week, for most of their lifetimes. The carcinogenicity of PCE in humans has not been extensively studied; however, an increase in the incidence of cancer has been noted in dry cleaners working with PCE (3,4). Based upon the animal tests, PCE may be considered a potential carcinogen.

Signs and symptoms of overexposure include malaise, dizziness, headache, increased perspiration, fatigue, incoordination and impaired mental acuity (5).

As of June, 1986, CAL/OSHA has reduced the exposure limit in the workplace from 100 ppm to 50 ppm as a time-weighted average over an 8 hour workshift. They have further designated an excursion limit of 200 ppm for no more than 5 minutes in any 3 hour period, and a ceiling of 300 ppm. The ACGIH has set its Threshold Limit Value for exposure at 50 ppm for an 8-hour day, and has also set 200 ppm as a short-term exposure limit. NIOSH has also recommended 50 ppm as an 8-hour limit. It should be noted that these limits are based upon information derived from acute, high-level exposure incidents, not long-term, low-level exposures.

Uptake and Metabolism

The major route of absorption of PCE is through the Lung: BO % to 90 % of inhaled vapor is absorbed (6). Skin exposure can appreciably increase absorption. For example, immersion of one thumb in PCE gives an exposure equivalent to breathing about 10 ppm (7). Additionally, exercising while exposed increases uptake by 50 % to 300 % or more as compared to a resting state (6,8).

The excretion of PCE is mostly (80-98%) through exhalation of the unchanged compound through the lung. About 2 % of an absorbed dose is metabolized to trichloroacetic acid (TCA), which is excreted in the urine. TCA, because of its binding to serum albumin, can be detected in the blood or urine for a fairly long time, and has a half-life of about three days. It is important to note that the metabolism of PCE to trichloroacetic acid is inhibited by ethanol use (9); thus, a low TCA level cannot be used to assure safe exposure levels of PCE if the victim also uses alcohol.

The half-life of PCE in the blood is not simply determined. Initially, within a few hours of typical occupational exposure, the concentration of PCE measured in blood or expired air drops rapidly, with a half-life of just a few hours (10). However, one or two days after exposure has ceased, the decline of PCE levels measured in the same way becomes much slower, with a half-life approaching 3 days. Other phases of excretion are still unknown.

There is more fat storage of PCE than other chlorinated solvents such as trichoroethylene or methyl chloroform. This may be responsible for its complex excertion behavior (11). Due to this fat storage, repeated exposures generally give rise to higher blood levels of PCE as measured a few days after exposure, than do single exposures.

Biological Monitoring

A method of biological monitoring has been proposed by Monster (12) which would assure with 95% confidence that exposure over a 40 hour workweek does not exceed 50 ppm in the air. Determinations can be based on taking a sample of blood, urine, or expired air 15-30 minutes after the end of a Friday workshift ("end-of the-week shift"). The proposed levels are.

BLOOD PERCHLOROETHYLENE 1,390 ppb (meg/i) BLOOD TRICHLOROACETIC ACID 326 ppb (meg/i) URINARY TRICHLOROACETIC ACID 4.2 mg/gm creatinine EXPIRED AIR PERCHLOROETHYLENE 12.5 ppm.

The ACGIH recently announced an intent to establish Biological Exposure Indices (BEI) for Perchloroetheylene which are similar to these proposed levels. It should be noted that these are conservative and on the average will be exposed to 50 ppm of PCE. The average blood PCE levels expected at the end of a Friday workshift will be about 2,000 to 3,000 ppb after a week's exposure to 50 ppm in the air (6).

Because of its widespread use in society, almost everyone is exposed to low levels of PCE. Drinking water is occasionally found to have a few micrograms per liter of PCE, and persons living near dry cleaning facilities may breathe concentrations in the air of up to 0. 15 ppm(l3). Air near old chemical disposal sites can have air concentrations estimated to be a few parts per billion (14), which would be expected to cause blood levels of about 0.5 to 1.0 ppb.

For information on sampling procedures, please see the Pacific Toxicology Laboratories collection and ship ping instructions for urine and blood volatiles.



(1) Monster (1983) **The proposed biological threshold is a blood level, drawn at the end of a Friday workshift, which would assure that exposures were under 50 ppm during the workweek.

(2) Monster (1979)

(3) Monster (1970)

References

1.) Axelson, O., et. al., Current Aspects of Solvent Related Disorders. In Developments in Occupational Medicine (ed. Carl Zenz), Yearbook Medical Publishers Inc. , Chicago, Pp. 237-59, 1977.

2.) National Toxicology Program. Technical Report, Approved Final Draft; Toxicology and carcinogenesis studies of tetrachloroethylene (perchloroethylene) in F344/N and B6C3F1 mice (inhalation studies). National Toxicology Program, National Institute of Health, Public Health Service, U.S. Department of Health and Human Services, August, 1985.

3.) Apfeldorf, R. and Infante, P., Review of epidemiologic study results of vinyl chloride related compounds, Environ. Health Perspect. 41: 221-26, 1981.

4.) Milham, S., Occupational mortality in Washington State: 1950-1971, HEW No. 76-175-C.

5.) Sittig, M., Handbook of~I~xic and Hazardous Chemicals, Noyes Publications, 1981.

6.) Monster, A.C., Tetrachloroethylene. In Biological Monitoring and Surveillance of Workers Exposed to Chemicals, Eds. Aitio, A., Riihimiaki, V., and Vainio, H., McGraw-Hill, 1984.

7.) Hake, C.L. and Stewart, R.D., Human exposure to tetrachloroethvlene.· Inhalation and skin contact, Environ. l-Iealth Perspect. 21: 231-238, 1977.

8.) Monster, A.C., Boersma, G., and Steenweg, H., Kinetics of tetrachloroethylene in volunteers: Influence of exposure concentration and workload, Int. Arch. Occup. Environ. Health. 42: 303-309, 1979.

9.) Reichert, D., Biological actions and interactions of tetrachloroethylene, Mutation Research 123:411-429, 1983.

10.) Stewart, R.D., Baretta, E.D., Dodd, H.C., and Torkelson, T.R., Experimental human exposure to tetrachloroethylene, Arch. Environ. Health 20:224-229, 1970.

11.) Savolainen, H., Pharmacokinetics, pharmacody namics, and aspects ofneurotoxic effect offour inhaled aliyphatic chlorohydrocarbon solvents as relevant in man, fur. J. Drug Metab. Pharm. 6:85-90, 1981.

12.) Monster, A.C., Regouin-Peeters, W., van Schijndel, A., and van der Tuin, J ., Biological monitoring of occupational exposure to tetrachloroethylene, Scand. J. Work Environ. Health 9:273-281, 1983.

13.) Verberk, h/l.M. and Scheffers, T.M.L., Tetrachloroethvlene in exhaled air of residents near dry-cleaning shops, Environmental Research. 21:432-437, 1980.

14.) Monster, A.C. and Smolders, J.F.J., Tetrachloroethylene in exhaled air of persons living near polluted sources, Int. Arch. Occup. Environ. Health 53:331-336, 198413.

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